Serum sodium concentration in sickle cell patient | Blazingprojects Postgraduate Thesis
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Serum sodium concentration in sickle cell patient

 

Table Of Contents


Chapter ONE

INTRODUCTION

  • 1.1Introduction
  • 1.2Background of Study
  • 1.3Problem Statement
  • 1.4Objective of Study
  • 1.5Limitation of Study
  • 1.6Scope of Study
  • 1.7Significance of Study
  • 1.8Structure of the Research
  • 1.9Definition of Terms

Chapter TWO

LITERATURE REVIEW

  • 2.1Overview of Sickle Cell Disease
  • 2.2Serum Sodium Concentration in Health and Disease
  • 2.3Relationship Between Sickle Cell Disease and Serum Sodium
  • 2.4Impact of Serum Sodium on Sickle Cell Patient Outcomes
  • 2.5Current Treatment Approaches for Managing Serum Sodium in Sickle Cell Patients
  • 2.6Studies on Serum Sodium Levels in Sickle Cell Disease
  • 2.7Challenges in Monitoring Serum Sodium in Sickle Cell Patients
  • 2.8Future Research Directions in Understanding Serum Sodium in Sickle Cell Disease
  • 2.9Global Perspectives on Sickle Cell Disease and Serum Sodium
  • 2.10Summary of Literature Review

Chapter THREE

RESEARCH METHODOLOGY

  • 3.1Research Design and Methodology
  • 3.2Selection of Study Participants
  • 3.3Data Collection Methods
  • 3.4Serum Sodium Measurement Techniques
  • 3.5Statistical Analysis Procedures
  • 3.6Ethical Considerations
  • 3.7Limitations of the Research Methodology
  • 3.8Validation Methods for Study Findings

Chapter FOUR

DATA PRESENTATION AND ANALYSIS

  • 4.1Overview of Study Findings
  • 4.2Serum Sodium Levels in Sickle Cell Patients
  • 4.3Factors Influencing Serum Sodium Concentration
  • 4.4Comparison with Healthy Controls
  • 4.5Impact on Clinical Outcomes
  • 4.6Treatment Strategies and Recommendations
  • 4.7Discussion on Potential Mechanisms
  • 4.8Implications for Future Research

Chapter FIVE

SUMMARY, CONCLUSION AND RECOMMENDATIONS

  • 5.1Summary of Research Findings
  • 5.2Conclusion and Interpretation of Results
  • 5.3Contributions to the Field
  • 5.4Recommendations for Clinical Practice
  • 5.5Implications for Public Health
  • 5.6Future Research Directions
  • 5.7Reflection on the Research Process
  • 5.8Closing Remarks and Acknowledgments

Thesis Abstract

Sickle cell disease (SCD) is a group of inherited disorders of the beta-hemoglobin chain. Normal hemoglobin has 3 different types of hemoglobin – hemoglobin A, A2, and F. Hemoglobin S in sickle cell disease contains an abnormal beta globin chain encoded by a substitution of valine for glutamic acid on chromosome 11 (Bunn,2007). This is an autosomal recessive disorder. Sickle cell disease refers to a specific genotype in which a person inherits one copy of the HbS gene and another gene coding for a qualitatively or quantitatively abnormal beta globin chain. Sickle cell anemia (HbSS) refers to patients who are homozygous for the HbS gene, while heterozygous forms may pair HbS with genes coding for other types of abnormal hemoglobin such as hemoglobin C, an autosomal recessive mutation which substitutes lysine for glutamic acid. In addition, persons can inherit a combination of HbS and β-thalassemia. The β-thalassemias represent an autosomal recessive disorder with reduced production or absence of β-globin chains resulting in anemia. Other genotype pairs include HbSD, HbSO-Arab and HbSE (Meremiku, 2008).

Sickle hemoglobin in these disorders cause affected red blood cells to polymerize under conditions of low oxygen tension resulting in the characteristic sickle shape. Normal red cells live about 120 days in the blood stream but sickled red cells die after about 10 – 20 days. Because they cannot be replaced fast enough, the blood is chronically short of red blood cells, a condition called anaemia. Aggregation of  sickle cells in the microcirculation from inflammation, endothelial abnormalities, and  thrombophilia lead to ischemia in end organs and tissues distal to the blockage (Hayes, 2004).


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